Alterations in thigh subcutaneous adipose tissue gene expression in protease inhibitor-based highly active antiretroviral therapy

Chaparro, Juan D.; Reeds, Dominic N.; Wen, Weidong; Xueping, E.; Klein, Samuel; Semenkovich, Clay F.; Bae, Kyongtae T.; Quirk, Erin; Powderly, William G.; Yarasheski, Kevin E.; Li, Ellen

doi:10.1016/j.metabol.2004.08.022

Cited by 31 publications

(26 citation statements)

References 33 publications

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“…63 There are no studies that have compared regional leptin mRNA expression in subcutaneous adipose tissue; however, there are indirect suggestions that basal expression does not differ between abdominal and gluteofemoral fat. 64,65 Serum leptin increases in parallel with BMI and, interestingly, is higher in women. [66][67][68][69][70] The sexual dimorphism in circulating leptin levels is apparent already in childhood 71,72 and has been attributed to differences in subcutaneous fat mass and adipocyte cell size.…”

Section: Leptinmentioning

confidence: 97%

Gluteofemoral body fat as a determinant of metabolic health

2010

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Body fat distribution is an important metabolic and cardiovascular risk factor, because the proportion of abdominal to gluteofemoral body fat correlates with obesity-associated diseases and mortality. Here, we review the evidence and possible mechanisms that support a specific protective role of gluteofemoral body fat. Population studies show that an increased gluteofemoral fat mass is independently associated with a protective lipid and glucose profile, as well as a decrease in cardiovascular and metabolic risk. Studies of adipose tissue physiology in vitro and in vivo confirm distinct properties of the gluteofemoral fat depot with regards to lipolysis and fatty acid uptake: in day-to-day metabolism it appears to be more passive than the abdominal depot and it exerts its protective properties by long-term fatty acid storage. Further, a beneficial adipokine profile is associated with gluteofemoral fat. Leptin and adiponectin levels are positively associated with gluteofemoral fat while the level of inflammatory cytokines is negatively associated. Finally, loss of gluteofemoral fat, as observed in Cushing's syndrome and lipodystrophy is associated with an increased metabolic and cardiovascular risk. This underlines gluteofemoral fat's role as a determinant of health by the long-term entrapment of excess fatty acids, thus protecting from the adverse effects associated with ectopic fat deposition.

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Section: Leptinmentioning

confidence: 97%

Gluteofemoral body fat as a determinant of metabolic health

2010

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“…RNA was isolated by Trizol (Invitrogen) from treated cell lines quantitative real-time PCR was conducted using the method as described previously (37). Briefly, 2 μg of total RNA per sample were converted to cDNA using the SuperScript First-Strand Synthesis system for reverse transcription-PCR (Invitrogen).…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

Chemopreventive Effects of Pioglitazone on Chemically Induced Lung Carcinogenesis in Mice

Wang

James

Wang

et al. 2010

Molecular Cancer Therapeutics

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Pioglitazone [(RS)-5-(4-[2-(5-ethylpyridin-2-yl)ethoxy]benzyl)thiazolidine-2,4-dione] is a ligand of nuclear receptor peroxisome proliferator-activated receptor γ that is approved for the treatment of type II diabetes mellitus. Activation of peroxisome proliferator-activated receptor γ has been associated with anticancer activities in a variety of cancer cell lines through inhibition of proliferation and promotion of apoptosis. We examined the effect of pioglitazone on lung cancer development in carcinogen-induced lung adenocarcinoma and squamous cell carcinoma (SCC). When pioglitazone was administered beginning 8 weeks after the first carcinogen treatment when microscopic adenomas already existed, pioglitazone significantly inhibited tumor load (sum of tumor volume per lung in average) by 64% (P < 0.05) in p53 wt/wt mice and 50% (P < 0.05) in p53 wt/Ala135Val mice in the lung adenocarcinoma model. Delayed administration of pioglitazone caused a limited (35%, P < 0.05) decrease in lung SCC. Induction of apoptosis occurred in both model systems. These data show that pioglitazone significantly inhibited progression of both adenocarcinoma and SCC in the two mouse model systems. Mol Cancer Ther; 9(11); 3074-82. ©2010 AACR.

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“…Relative gene expressions of EGFR (NM_207655), VEGFR (NM_008029), FGFR (NM_008010), platelet-derived growth factor receptor (NM_011058), and IGFR (NM_010513) were determined by quantitative real-time PCR analysis (33). The primers shown on Table 5 were designed using PrimerExpress version 2.0 (Applied Biosystems, Foster City, CA).…”

Section: Quantitative Real-time Pcr Analysismentioning

confidence: 99%

Effect of an Epidermal Growth Factor Receptor Inhibitor in Mouse Models of Lung Cancer

Yan¹,

Lü²,

Wang³

et al. 2006

Molecular Cancer Research

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Gefitinib (Iressa, ZD1839) is a potent high-affinity competitive tyrosine kinase inhibitor aimed primarily at epidermal growth factor receptor (EGFR). Inhibitors in this class have recently been approved for clinical use in the treatment of advanced non -small cell lung cancer as monotherapy following failure of chemotherapy. We examined the efficacy of gefitinib on lung tumorigenesis in mouse models using both postinitiation and progression protocols. Gefitinib was given at a dose of 200 mg/kg body weight (i.g.) beginning either 2 or 12 weeks following carcinogen initiation. In the postinitiation protocol, gefitinib significantly inhibited both tumor multiplicity (f70%) and tumor load (f90%) in A/J or p53-mutant mice (P < 0.0001). Interestingly, gefitinib was also highly effective against lung carcinogenesis in the progression protocol when individual animals already have multiple preinvasive lesions in the lung. Gefitinib exhibited f60% inhibition of tumor multiplicity and f80% inhibition of tumor load when compared with control mice (both P < 0.0001). These data show that gefitinib is a potent chemopreventive agent in both wild-type and p53-mutant mice and that a delayed administration was still highly effective. Analyses of mutations in the EGFR and K-ras genes in lung tumors from either control or treatment groups showed no mutations in EGFR and consistent mutation in K-ras. Using an oligonucleotide array on control and gefitinib-treated lesions showed that gefitinib treatment failed to alter the activity or the expression level of EGFR. In contrast, gefitinib treatment significantly altered the expression of a series of genes involved in cell cycle, cell proliferation, cell transformation, angiogenesis, DNA synthesis, cell migration, immune responses, and apoptosis. Thus, gefitinib showed highly promising chemopreventive and chemotherapeutic activity in this mouse model of lung carcinogenesis. (Mol Cancer Res 2006;4(12):971 -81)

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Alterations in thigh subcutaneous adipose tissue gene expression in protease inhibitor-based highly active antiretroviral therapy

Cited by 31 publications

References 33 publications

Gluteofemoral body fat as a determinant of metabolic health

Gluteofemoral body fat as a determinant of metabolic health

Chemopreventive Effects of Pioglitazone on Chemically Induced Lung Carcinogenesis in Mice

Effect of an Epidermal Growth Factor Receptor Inhibitor in Mouse Models of Lung Cancer

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